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1                                              aPTTs were collected 6, 12, and 24 hours after thromboly
2 rison, the coagulation times of the acoustic aPTT and PiCT yielded an excellent correlation with the
3                        Finally, the acoustic aPTT assay is the ''gold standard'' for a dose administr
4            Before drug administration, ACTs, aPTTs, and hemodynamics were similar among the groups.
5 in were significantly more likely to have an aPTT measurement in the target range (P < .0001).
6 en glycosidase-treated FV was analyzed in an aPTT (activated partial thromboplastin time)-based APC s
7 ected by routine clinical evaluation with an aPTT assay.
8                                  The ACT and aPTT are sensitive to IV dalteparin at clinically releva
9  and 30 minutes after drug infusion, ACT and aPTT were slightly higher in those receiving rPF4, but t
10 After plasma transfusion, the median INR and aPTT changes were -0.2 and -5, respectively.
11  of a year in the three animals studied, and aPTT mixing studies showed no evidence for neutralizing
12 lant activity in an in vitro clotting assay (aPTT EC1.5x = 0.27 muM) and excellent selectivity agains
13            Although the relationship between aPTT and clinical outcome was confounded to some degree
14 ticoagulant activity measured by whole blood aPTT.
15                                         Both aPTT and anti-factor Xa increased with escalating doses
16 ence of baseline prognostic characteristics, aPTTs higher than 70 seconds were found to be associated
17 icient plasma when assessed by the classical aPTT coagulation assay.
18                                          For aPTT we report for the first time that a QCM-D (Quartz C
19                                          For aPTT, previously reported associations with KNG1, HRG, F
20 identified a new independent association for aPTT in F5 (rs2239852, P-value = 1.9 x 10(-8)), which cl
21  reliable than the standard coagulometer for aPTT range of upper limits of coagulation times.
22                                 The GWAS for aPTT was conducted in 9,240 individuals of European ance
23 d meta-analysis to identify genetic loci for aPTT and PT.
24 tudy (GWAS) has been reported previously for aPTT, but no GWAS has been reported for PT.
25 s that have not been previously reported for aPTT.
26 onducted a genome-wide association study for aPTT and identified significant associations with SNPs i
27 We conducted a genetic association study for aPTT in 9719 EAs and 2799 AAs from the Atherosclerosis R
28                                Markedly high aPTTs were associated with increased risk of TIMI major
29                                Markedly high aPTTs were more likely in patients who were older (adjus
30                                       Higher aPTT at 24 hours was strongly related to lower patient w
31          The present study aimed to identify aPTT-related gene variants in both European Americans (E
32 m has the potential to significantly improve aPTT control of intravenous heparin compared with curren
33 unt for approximately 29% of the variance in aPTT and two loci that account for approximately 14% of
34  approximately 18% of phenotypic variance in aPTT in the Lothian Birth Cohorts.
35 e, and 11 studies used a range that included aPTT values 1.5 times the control value.
36                  Genetic factors influencing aPTT are not well understood, especially in populations
37 d a fibrin-specific lytic and had an initial aPTT drawn within 4 to 8 hours of starting therapy.
38 to recommended dosing, only 33.8% of initial aPTTs were therapeutic (1.50 to 2.00 times control); 13.
39 rs (odds ratio, 2.11; P=0.004); markedly low aPTTs tended to be associated with increased risk of fat
40 rol value are subtherapeutic for most modern aPTT reagents.
41 r IX resulted in normalization of a modified aPTT in mouse plasma.
42                                         Most aPTT values were above therapeutic range or beyond measu
43 rombin (for anti-Xa), and baseline levels of aPTT and ACT, respectively.
44                         Of the 344 end-point aPTT measurements, 78% were within +/-10 seconds of the
45 icted massive RBC transfusion better than PT/aPTT or INR (P < 0.001).
46            This is the first study to report aPTT-related genetic variants in AAs.
47 /h, with dose adjustment to achieve a target aPTT of 60 to 85 seconds.
48                 The time to achieve a target aPTT was 93 minutes without and 150 minutes with an init
49 usted the heparin infusion to reach a target aPTT.
50                                          The aPTT levels in the OHEP/SNAC group peaked at 30 minutes
51                                          The aPTT, anti-Xa and anti-IIa activities, and TFPI concentr
52 al and analyzed the relationship between the aPTT and both baseline patient characteristics and clini
53 n unexpected direct relationship between the aPTT and the risk of subsequent reinfarction.
54 til proven otherwise, we should consider the aPTT range of 50 to 70 seconds as optimal with intraveno
55                             At 12 hours, the aPTT associated with the lowest 30-day mortality, stroke
56             By contrast, prolongation of the aPTT requires neither antithrombin nor heparin cofactor
57 in-antithrombin reaction and may prolong the aPTT by interfering with activation of factor VIII, ther
58 i-Xa, activated partial thromboplastin time (aPTT) and activated clotting time (ACT); (2) other facto
59   The activated partial thromboplastin time (aPTT) and anti-factor X (anti-Xa) levels were measured.
60       Activated partial thromboplastin time (aPTT) and prothrombin time (PT) are clinical tests commo
61 in an activated partial thromboplastin time (aPTT) assay and was activated by factor XIa more slowly
62 ty in activated partial thromboplastin time (aPTT) assays.
63 on of activated partial thromboplastin time (aPTT) before and after the treatment.
64 stage activated partial thromboplastin time (aPTT) clotting assay (36% +/- 9.6% of FVIII WT) and a va
65 , the activated partial thromboplastin time (aPTT) coagulation assay was performed, and the viscosity
66 d the activated partial thromboplastin time (aPTT) in 29,656 patients in the Global Utilization of St
67 duced activated partial thromboplastin time (aPTT) is a risk marker for incident and recurrent venous
68       Activated partial thromboplastin time (aPTT) is associated with risk of thrombosis and coagulat
69 ) and activated partial thromboplastin time (aPTT) obtained before elective surgery with initial PT a
70 arget activated partial thromboplastin time (aPTT) of 55 to 85 seconds and were administered for 96 h
71 lets, activated partial thromboplastin time (aPTT) reagent and prothrombin time reagent and reduces t
72 f the activated partial thromboplastin time (aPTT) therapeutic range is required to ensure administra
73 ) and activated partial thromboplastin time (aPTT) values were 1.5 and 48, respectively.
74  with activated partial thromboplastin time (aPTT) was tested for the top SNPs.
75 d the activated partial thromboplastin time (aPTT) when added to normal plasma, and alter the kinetic
76 f the activated partial thromboplastin time (aPTT), and that injection of 10(11) particles of an aden
77 ECT), activated partial thromboplastin time (aPTT), and thrombin time (TT) were secondary endpoints a
78 es in activated partial thromboplastin time (aPTT), anti-factors IIa and Xa, and tissue factor pathwa
79  (PT)/activated partial thromboplastin time (aPTT), international normalized ratio (INR), platelet co
80 f the activated partial thromboplastin time (aPTT), over controls (P < 0.05).
81 ron), activated partial thromboplastin time (aPTT), plasma anti-Xa and anti-IIa levels, tissue factor
82 s for activated partial thromboplastin time (aPTT).
83 ) and activated partial thromboplastin time (aPTT).
84 , and activated partial thromboplastin time [aPTT]) have remained at the upper limits of the normal r
85 y ''activated Partial Thromboplastin Time'' (aPTT) and ''Prothrombinase complex-induced Clotting Test
86 ving activated partial thromboplastin times (aPTTs) within a range of 55 to 85 seconds in recent tria
87 ored activated partial thromboplastin times (aPTTs).
88 ction to less than 30 000 U/d in response to aPTT results.
89              Only 3 studies used a validated aPTT therapeutic range, and 11 studies used a range that
90  R(2)=0.98 in calibration curves) along with aPTT from frequency and dissipation shifts together in a
91 rs710446 and rs4253417) also associated with aPTT.
92                                     Anti-Xa, aPTT, and ACT all showed good discrimination between UFH
93 urred in anti-factor IIa and anti-factor Xa. aPTT rose from 28+/-0.5 to 42.2+/-6.3 seconds 2 hours af

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